Traumatic memory
Traumatic Memory are memories that are characterized by fragmented and intense sensations and emotions, often with little or no episodic memory attached. When the state of hyper-arousal and neurophysiological activation associated with a traumatic event persists, the brain changes (Perry 1988, Perry 1991). In much the same way that repeated exposure to a cognitive stimulus results in a cognitive memory, repeated or continuous exposure to this state of arousal results in a 'state memory'. The system has been in the aroused state so much that the brain, likely using the same molecular mechanisms underlying learning/memory (Kandel 1989), has readjusted to these new environmental demands. The arousal is no longer reversible; there is a new homeostatic set point for neurotransmitter systems (e.g., norepinephrine, epinephrine) in the brain which regulate arousal, attention, affect and sympathetic nervous system functioning (Perry 1991). These 'state memories' are the basis for the characteristic symptoms in PTSD. The hypervigilance, increased startle, affective lability, anxiety, dysphoria, and the increased SNS activity and reactivity can all be related to the altered functioning key neurotransmitter systems in the brain (see Krystal et al., 1989; Perry et al., 1990; Perry 1991). Measurement Instruments # Traumatic Memory Inventoryvan der Kolk, B., Hopper, J., Osterman, J., (2001). Exploring the nature of traumatic memory, Journal of aggression, maltreatment and trauma, 4(2), 9-31. Clinical formulation Traumatic memories, if pervasive and chronic, may lead to Complex post traumatic stress disorder. Since episodes may lead to Post traumatic stress disorder. Treatment EMDR has been shown to be one effective method or resolving traumatic memories and reducing the clinical symptoms that may result. See also Complex post traumatic stress disorder Post traumatic stress disorder References Bibliography Breier, A., Albus, M., Pickar, D., Zahn, T. P., Wolkowitz, O.M., Paul, S. M. (1987). Controllable and uncontrollable stress in humans: alterations in mood and neuroendocrine and psychophysiological function. Am. J. Psychiatry, 144:11, 1419-1425. Breier, A. B., Kelsoe, J. R., Kirwin, P. D., Beller, S., Wolkowitz, O. M., Pickar, D. (1988). Early parental loss and development of adult psychopathology. Arch. Gen. Psychiatry, 45: 987-993. Cannon, W. B. (1914). The emergency function of the adrenal medulla in pain and the major emotions. Am. J. Physiol. 33: 356-372. Kandel ER (1989) Genes, nerve cells, and remembrance of things past. J. Neuropsychiatry Clin. Neurosci.1: 103-125. Krystal, J.H., Kosten, T., Perry, B.D., Mason, J., Southwick, S. and Giller, E.L. (1989) Neurobiological aspects of post-traumatic stress disorder: review of clinical and preclinical studies. Behavior Therapy 20: 177-198. Perry, B.D. (1988) Placental and blood element neurotransmitter receptor regulation in humans: potential models for studying neurochemical mechanisms underlying behavioral teratology. Prog Brain Res 73: 189-206. Perry, B.D. (199) Neurobiological sequelae of childhood trauma: Post traumatic stress disorders in children. In (M. Murberg, Ed.) Catecholamines in Post traumatic Stress Disorder: Emerging Concepts. American Psychiatric Press, Inc., Washington, DC pp 100-128. Perry, B. D., Southwick, S. M., Giller, E. J. (1990). Adrenergic receptors in posttraumatic stress disorder. In: (E. L. Giller, Ed.) Biological Assessment and Treatment of Posttraumatic Stress Disorder. American Psychiatric Press, Inc., Washington, DC pp 89-114 Selye, H. (1936). A syndrome produced by diverse nocuous agents. Nature, 138:32. Wolf, W.E., Mosnaim A.D. (Eds) Post traumatic Stress Disorder : Biological Mechanisms and Clinical Aspects. American Psychiatric Press, Inc, Washington, DC, 1990.